Treating Tick borne infections

Insights From the Field: Treating Lyme Disease and Other Tick- Borne Illnesses Allison Nguyen; Nikki Kean | April 3, 2026 Vanessa Pomarico-Denino, EdD, APRN, FNP-BC, FAANP, contracted Lyme disease and babesiosis not while out in the woods, but while sitting on the paved patio in her mother’s backyard. At the same time, her mother was critically ill in the hospital, being treated for a tick-borne illness. Dr Pomarico-Denino, a nurse practitioner (NP) living in Connecticut, draws on her personal experience and clinical expertise to educate others on the treatment and prevention of tick-borne illnesses. She serves as the lead clinician for diversity, equity, inclusion, and belonging for the Northeast Medical Group and teaches for Fitzgerald Health Education Associates, which has been educating NPs for 32 years. With the rise in Lyme disease cases in the United States, it is increasingly important for health care professionals to stay current with the latest treatment recommendations. 1 In addition, Dr Pomarico-Denino urges clinicians to test and treat for the other 3 most common tick-borne illnesses: babesiosis, ehrlichiosis, and anaplasmosis. “Patients can typically be infected with more than one type of infection. If you test just for Lyme disease, you are missing other infection(s).” Epidemiology of Lyme Disease in the United States https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 1 of 8Lyme disease first became a nationally notifiable condition in the US in 1991. According to the Centers for Disease Control and Prevention (CDC), approximately 476,000 people in the country are diagnosed and treated for Lyme disease annually. 1 This estimate includes patients treated based on clinical suspicion of Lyme disease. In 2023, over 89,000 cases of Lyme disease were reported to the CDC by state health departments and the District of Columbia, representing a significant increase from the 2019 to 2022 average of 46,115 cases. 2 While a portion of the increase in cases is attributed to changes in surveillance methods, Lyme disease remains the most common tick-borne illness in the US. 3,4 Dr Pomarico-Denino said that this approximation is likely an underestimate, saying that “not all patients report cases unless they’re getting sick. Patients often come in with different complaints, but since this disease is always on my radar, I’ll run the blood work, and it sometimes shows they’ve had an old Lyme infection that may or may not have been treated.” Factors contributing to the increase in rates of Lyme disease include climate change and changes to human behavior, such as spending more time outdoors, which began during the COVID-19 pandemic. “I was taking ticks off of people all winter long because we didn’t have a prolonged, cold, hard frost [in the Northeast],” said Dr Pomarico-Denino. Climate change has also expanded the geographic range of ticks, allowing them to survive in environments that were previously inhospitable. 5 Ticks live on deer, rodents, birds, and other animals. In the US, Lyme disease and babesiosis, ehrlichiosis, and anaplasmosis are significantly more common in the Northeast, mid-Atlantic, and upper Midwest areas than in other regions of the country. 5 Guideline-Recommended Lyme Disease Treatment The CDC-recommended treatment regimens for Lyme disease align with the latest guidelines from the Infectious Diseases Society of America (IDSA) for the treatment of tickborne diseases. 6,7 In summation, the guidelines state that the recommended duration of therapy is 10 to 14 days for early Lyme disease, 14 days for Lyme carditis, https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 2 of 814 to 21 days for neurologic Lyme disease, and 28 days for late Lyme arthritis. “ The treatment for Lyme is doxycycline, which also covers ehrlichiosis and anaplasmosis, but babesiosis is treated with atovaquone plus azithromycin for at least 7 to 10 days, according to the CDC. ” Vanessa Pomarico-Denino, EdD, APRN, FNP-BC, FAANP There is some controversy regarding doxycycline administration in pediatric patients, noted Dr Pomarico-Denino. “Doxycycline is contraindicated in anyone under the age of 8 because of the risk of permanent tooth staining unless the infection is life-threatening, then the benefit outweighs the risk,” she said. “If doxycycline is used in children, the dose is 4.4 mg/kg with a maximum dose of 200 mg.” Recent studies state that doxycycline can be safely administered for short durations regardless of patient age. IDSA Treatment Guidelines for Tick-Borne Illnesses Tick-Borne Illness Treatment Treatment Duration Lyme Disease (Borrelia burgdorferi) Patients with high-risk a Ixodes scapularis bites in all age groups Oral doxycycline (200 mg) Single 200 mg dose within 72 hours of tick removal over observation Patients with erythema migrans Oral antibiotic therapy with doxycycline, amoxicillin, or cefuroxime axetil 10-day course of doxycycline, a 14-day course of amoxicillin, or cefuroxime axetil Anaplasmosis (Anaplasma phagocytophilum) Oral doxycycline 10-14 days Outpatient: Oral https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 3 of 8Babesiosis (Babesia microti) atovaquone 750 mg BID plus oral azithromycin 500 mg on day 1, then 250 mg for 7-10 days Inpatient: More severe disease requires 500-1000 mg of azithromycin daily 7-10 days Ehrlichiosis (Ehrlichia chaffeensis, E. ewingii, or E. muris eauclairensis ) Oral doxycycline 7-14 days, or until fever resolves a A tick bite is considered high risk only if it meets the following 3 criteria: the tick bite was from (a) an identified Ixodes spp. vector species, (b) it occurred in a highly endemic area, and (c) the tick was attached for ≥36 hours. Dr Pomarico-Denino said that the vast majority of patients are unable to determine how long a tick has been attached, so many providers typically prescribe a single- use dose of doxycycline as a precautionary measure. After treatment with doxycycline, it is recommended that patients follow up with their provider if symptoms of Lyme disease develop. These symptoms include erythema migrans (also commonly referred to as a bull’s-eye rash), flu-like symptoms, and severe headaches. 8 “Only about 70% of people with Lyme infections get a rash, and 30% don’t ever get a rash or they get a rash in an area that you wouldn’t see it,” said Dr Pomarico-Denino. “If patients develop symptoms like this, then we test them sooner and start them on a longer course of doxycycline. We no longer immediately put people on 3 weeks of doxycycline because of one bite, because not all ticks are infected.” Read more: Leptospirosis Approach to Treating Coinfections with Lyme Disease https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 4 of 8While patients with Lyme disease usually respond to antibiotic treatment, approximately 10% to 20% of reported patient cases experience continued symptoms despite treatment. Of these patients, approximately 50% will experience a coinfection, requiring a reevaluation of the treatment approach. 9,10 “Ticks can carry more than one kind of infection, and patients are often infected with more than one type of infection,” Dr Pomarico-Denino said. “The treatment for Lyme is doxycycline, which also covers ehrlichiosis and anaplasmosis, but babesiosis is treated with atovaquone plus azithromycin for at least 7 to 10 days, according to the CDC.” Depending on the type of coinfection, the treatment approach for Lyme disease can differ. “Babesiosis can be significantly more life-threatening, especially if a patient’s parasite count increases and if they are elderly,” noted Dr Pomarico-Denino. “Many patients are hospitalized if they have other comorbid conditions, so we typically treat all conditions at the same time. But again, the treatment approach would change based on the patient,” she said. “Do I want to treat babesiosis the first week and then start the doxycycline? Or are we going to treat them all at the same time?” Preventing Tick Bites Per the IDSA guidelines, personal protective measures for preventing tick bites and tick-borne infections include N, N-diethyl-meta-toluamide (DEET), picaridin, ethyl-3- (N-butyl-N-acetyl) aminopropionate (IR3535), oil of lemon eucalyptus (OLE), p- methane-3,8-diol (PMD), 2-undecanone, or permethrin. “Permethrin comes in a spray that patients can spray on their clothing,” says Dr Pomarico-Denino. “We tell them not to put it on their skin since it’s very caustic, but they can put it on their shoes, hiking gear, hats, and backpacks. It lasts through 5 or 6 washings. They can get that at any garden center or order it on the permethrin website.” From Dr Pomarico-Denino’s personal experience living in a highly endemic area for https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 5 of 8ticks, some additional recommendations she has include tucking in clothing, wearing hats, and conducting a thorough skin survey once you have returned home. A recommendation for patients who are avoiding chemical repellents includes using essential oils (eg, a mixture of thyme, citronella, and oregano oil) as a tick deterrent, although limited data support this approach. There are currently no vaccines available for Lyme disease. LYMERix ® , the only vaccine previously available in the US, was discontinued in 2002 because of low demand. One vaccine candidate, VLA15, is currently in Phase 3 clinical trials. Additionally, a human monoclonal antibody for pre-exposure prophylaxis (PrEP) for Lyme disease is expected to begin human trials soon. 11 Hear directly from Dr Vanessa Pomarico-Denino as she reminds clinicians to be on the lookout for lesser-known tick-borne infections, especially during the warmer months: This article originally appeared on Clinical Advisor References: 1. Lyme Disease Surveillance and Data. Centers for Disease Control and https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 6 of 82. 3. 4. 5. Prevention. Published March 13, 2025. Accessed August 2, 2025. https://www.cdc.gov/lyme/data-research/facts-stats/index.html Tickborne Disease Surveillance Data Summary. Published July 15, 2024. Accessed August 2, 2025. https://www.cdc.gov/ticks/data-research/facts- stats/tickborne-disease-surveillance-data-summary.html Kugeler KJ, Earley A, Mead PS, Hinckley AF. Surveillance for Lyme disease after implementation of a revised case definition — United States, 2022. MMWR Morb Mortal Wkly Rep. doi:10.15585/mmwr.mm7306a1 Nathavitharana RR, Mitty JA. Diseases from North America: focus on tick- borne infections. Clin Med (Lond) . doi:10.7861/clinmedicine.14-6-74 Climate Change Indicators: Lyme Disease. Environmental Protection Agency. Updated on June 13, 2025. Accessed August 3, 2025. https://www.epa.gov/climate-indicators/climate-change-indicators-lyme- disease 6. 7. 8. 9. 10. Clinical Care of Lyme Disease. Centers for Disease Control and Prevention. Published May 15, 2025. Accessed August 2, 2025. https://www.cdc.gov/lyme/hcp/clinical-care/index.html Lantos PM, Rumbaugh J, Bockenstedt LK, et al. AAN/ACR/IDSA 2020 guidelines for the prevention, diagnosis and treatment of Lyme disease. Clin Infect Dis . Published November 30, 2020. Accessed August 2, 2025. doi:10.1093/cid/ciaa1215 Signs and Symptoms of Untreated Lyme Disease. Centers for Disease Control and Prevention. Published May 15, 2024. Accessed August 2, 2025. https://www.cdc.gov/lyme/signs-symptoms/index.html Melia MT, Auwaerter PG. Time for a different approach to Lyme disease and long-term symptoms. N Engl J Med. Published March 31, 2016. doi:10.1056/NEJMe1502350 Johnson L, Wilcox S, Mankoff J, Stricker RB. Severity of chronic Lyme disease compared to other chronic conditions: a quality of life survey. PeerJ. Published March 27, 2014. doi:10.7717/peerj.322 https://www.dermatologyadvisor.com/features/treating-lyme-dis903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:22 AM Page 7 of 811. Lyme Disease Vaccine. Centers for Disease Control and Prevention. Published December 17, 2024. Accessed August 2, 2025. https://www.cdc.gov/lyme/about/lyme-disease-vaccine.html Sent from my iPhone Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574 Please excuse the shortness of this message, as it has been sent from a mobile device.

Rosacea Signos y Sintomas

Rosacea: Signs and Symptoms Colleen Stanton | April 17, 2026 Our easy-to-read fact sheets provide clinicians with reliable information to share with patients and their caregivers. Rosacea is a chronic inflammatory skin condition that causes redness, flushing, visible blood vessels, and small bumps on the face. 1 It most commonly affects the cheeks, nose, chin, and forehead. Rosacea tends to develop gradually. Many people first notice frequent flushing or blushing, which may later become persistent redness. Over time, additional symptoms such as visible blood vessels or acne-like bumps may appear. Although rosacea can affect anyone, it is most commonly seen in adults aged 30 to 50 years and is more frequently diagnosed in patients with fair skin. 2 However, it can occur in all skin types. While rosacea is not life-threatening, it can be a significant source of frustration or discomfort and negatively affect patients’ self-esteem, reducing overall quality of life. Signs and Symptoms of Rosacea Rosacea presents differently from person to person. Some patients may have only mild redness, while others experience more pronounced symptoms. Symptoms often flare up and then improve, rather than remaining constant. 3 Common signs and symptoms include the following: https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 1 of 10Common signs and symptoms include the following: Persistent facial redness, especially across the cheeks and nose; Flushing or blushing that occurs easily and frequently; Visible blood vessels; Small red bumps or pus-filled pimples; Burning, stinging, or sensitive skin; and Dry, rough, or swollen skin. More advanced cases may involve thickened skin, particularly on the nose, as well as ocular symptoms, including eye irritation, redness, or dryness. Types of Rosacea Rosacea is often grouped into subtypes based on the dominant symptoms, which guides treatment. Erythematotelangiectatic Rosacea (ETR) This type is characterized by persistent redness and visible blood vessels. Flushing is common and may worsen over time. Representing more than 50% of cases, ETR is the most prevalent form of rosacea. 1,4 Papulopustular Rosacea Often mistaken for acne, this type includes red bumps and pus-filled lesions along with background redness. Papulopustular rosacea accounts for about 43% of 3,4 cases. Ocular Rosacea https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 2 of 10Ocular Rosacea This form of rosacea involves inflammation of the ocular surface and eyelids, causing dryness, irritation, redness, and a gritty or burning sensation. It may occur on its own or alongside the more familiar skin symptoms of facial rosacea. 4,5 In some cases, eye symptoms can appear before skin changes develop, which can make ocular rosacea more difficult to recognize. Because the eyes are sensitive, even mild inflammation can lead to noticeable discomfort. Phymatous Rosacea This rarer type of rosacea leads to thickened, bumpy skin. It most commonly is seen on the nose and in men. Phymatous rosacea makes up about 7% of rosacea cases. 1,4 What Causes Rosacea? The exact cause of rosacea is not fully understood, but it is believed to involve a combination of factors. 2 Previous research has found that rosacea symptoms could be equally attributed to genetic and environmental factors. 6 Possible contributing factors include increased sensitivity of facial blood vessels, an overactive immune system, genetic predisposition, environmental triggers, and microorganisms on the skin such as Demodex mites. 5,6 Rosacea is not contagious and is not caused by poor hygiene. Common Triggers for Symptom Flares Many people with rosacea notice that certain factors trigger or worsen their symptoms. Identifying personal triggers is an important part of managing the condition. Common triggers include sun exposure, hot weather or cold wind, eating spicy https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 3 of 10foods, drinking alcohol (particularly red wine) or hot beverages, stress, emotional changes, exercise, and use of skin care products that irritate the skin. 1,6 Not all triggers affect everyone, so it can be helpful to track what seems to worsen your symptoms. Rosacea Diagnosis Rosacea is typically diagnosed through a clinical evaluation by a health care provider. There is no single test for rosacea. 1 During an evaluation, your provider may begin with examining your skin. They will ask for a complete medical history and will discuss triggers as well as symptom patterns. Early diagnosis can help prevent progression and make symptoms easier to manage. In some cases, additional testing may be done to rule out other skin conditions that can mimic rosacea. Distinguishing Rosacea From Other Skin Conditions Rosacea is often mistaken for other skin concerns. Understanding the differences can help you seek appropriate care. https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 4 of 10Rosacea vs Other Redness Farshchian M, Daveluy S. Rosacea. StatPearls Publishing; 2023. Accessed March 31, 2026. https://www.ncbi.nlm.nih.gov/books/NBK557574/ Rosacea vs Acne Rosacea and acne can look similar because both may involve red bumps and breakouts. However, redness and flushing are more prominent in rosacea, and patients may experience skin sensitivity or burning. Acne, on the other hand, commonly includes clogged pores, blackheads, and whiteheads. Acne affects a wider range of areas, including the back and chest. 7 Rosacea vs General Facial Redness Some people naturally have facial redness or flushing, but rosacea tends to be more persistent and progressive. With rosacea, redness may worsen over time. Visible blood vessels may develop, and additional symptoms such as bumps or irritation often occur. Simple redness without these features is less likely to be rosacea. https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 5 of 10Rosacea vs Eczema Eczema can also cause redness and irritation, but it typically presents differently. Patients with rosacea often experience burning or stinging, whereas eczema causes intense itching. Skin in patients with eczema may appear dry, cracked, or scaly. Eczema may affect areas beyond the face, such as the arms or behind the knees. While patients with some types of rosacea and eczema may both experience thickened skin, this symptom in patients with eczema is usually the result of itching and rubbing. 8 Rosacea vs Lupus Rash Another inflammatory disorder with skin symptoms that may be mistaken for rosacea is subacute cutaneous lupus erythematosus. This condition includes a butterfly-shaped rash across the cheeks and nose. Subacute cutaneous lupus erythematosus is associated with lupus, an autoimmune condition. Lupus rash is usually accompanied by other systemic symptoms, such as fatigue or joint pain, whereas rosacea symptoms are typically limited to the skin and eyes. Both conditions may cause visible blood vessels. 9 Managing Rosacea While rosacea cannot be cured, it can be effectively managed with the right approach. Treatment plans are tailored to each patient based on symptoms and disease severity. Management may involve gentle skin care products, over-the- counter topical treatments, antibiotics, laser and light therapy, and lifestyle modifications such as reducing sun exposure and alcohol intake. 10 Many people successfully manage their symptoms with a combination of medical care and lifestyle changes. https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 6 of 10lifestyle changes. Skin Care Strategies Gentle skin care is essential for people with rosacea. Recommendations include using mild, fragrance-free cleansers, avoiding harsh exfoliants or scrubs, and choosing products labeled for sensitive skin. Patients should apply a daily, broad- spectrum sunscreen with an SPF of 30 or higher. Consistency is key, and introducing new products slowly can help prevent irritation. 10 Medical Treatments A health care provider may recommend prescription or in-office treatments to help control symptoms. Options may include the following: Topical medications to reduce redness and inflammation; Oral medications, such as antibiotics, for more severe cases; Laser or light-based treatments to reduce visible blood vessels and flushing; and Topical eye drops or ointments for ocular rosacea; Treatment plans are often adjusted over time depending on how your skin responds. 10 Lifestyle Modifications Managing triggers plays an important role in reducing flare-ups. Helpful strategies include keeping a diary to identify personal triggers and practicing stress management techniques. Limiting exposure to extreme temperatures as well as using sunscreen or protective clothing outdoors may also help. Small adjustments can make a significant difference in symptom control. 10 https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 7 of 10When to See a Health Care Provider It is a good idea to seek medical advice if you: Notice facial redness that does not improve Experience frequent flushing or sensitivity Develop acne-like bumps that do not respond to over-the-counter treatments Have eye symptoms such as dryness or irritation Early evaluation can help confirm the diagnosis and prevent symptoms from worsening. Frequently Asked Questions Can rosacea go away on its own? Rosacea is a chronic condition, meaning it does not usually go away completely. However, symptoms can be controlled and improved with proper treatment and lifestyle adjustments. 3 What is the biggest trigger for rosacea? There is no single trigger that affects everyone. Common triggers include sun exposure, heat, alcohol, spicy foods, and stress. Identifying your personal triggers is key. 3 Can makeup make rosacea worse? https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 8 of 10Some makeup products may irritate sensitive skin. Choosing non-irritating, fragrance-free products designed for sensitive skin can help minimize flare-ups. 11 Can makeup disguise rosacea? For anyone with a desire to use makeup, choosing the correct products is important. Many dermatologists recommend water-based or powder makeup as these products are less likely to cause skin irritation. Makeup with a yellow tint may hide discoloration and a green tint may hide redness. 11 Is rosacea dangerous? Rosacea is not dangerous, but it can worsen over time if untreated. In some cases, it can affect the eyes or lead to thickened skin. Early management helps prevent complications. 1 Download this fact sheet as a PDF. 1. 2. 3. 4. References Farshchian M, Daveluy S. Rosacea. StatPearls Publishing; 2023. Accessed March 31, 2026. https://www.ncbi.nlm.nih.gov/books/NBK557574/ van Zuuren EJ, Arents BWM, van der Linden MM, Vermeulen S, Fedorowicz, Tan R. Rosacea: new concepts in classification and treatment. Am J Clin Dermatol. 2021;22(4):457-465. doi:10.1007/s40257-021-00595-7 Rainer BM, Kang S, Chien AL. Rosacea: epidemiology, pathogenesis, and treatment. Dermatoendocrinol. 2017;9(1):e1361574. doi:10.1080/19381980.2017.1361574 Barakji YA, Rønnstad ATM, Christensen MO, et al. Assessment of frequency of rosacea subtypes in patients with rosacea: a systematic review and meta- analysis. JAMA Dermatol. 2022;158(6):617-625. doi:10.1001/jamadermatol.2022.0526 https://www.dermatologyadvisor.com/factsheets/rosacea-signs-903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:19 AM Page 9 of 105. 6. 7. 8. 9. 10. 11. doi:10.1001/jamadermatol.2022.0526 Mohamed-Noriega K, Loya-Garcia D, Vera-Duarte GR, et al. Ocular rosacea: an updated review. Cornea. 2025;44(4):525-537. doi:10.1097/ICO.0000000000003785 Aldrich N, Gerstenblith M, Fu P, et al. Genetic vs environmental factors that correlate with rosacea: a cohort-based survey of twins. JAMA Dermatol. 2015;151(11):1213-1219. doi:10.1001/jamadermatol.2015.2230 Sutaria AH, Masood S, Saleh HM, Schlessinger J. Acne vulgaris. StatPearls Publishing; 2023. Accessed March 31, 2026. https://www.ncbi.nlm.nih.gov/books/NBK459173 Nemeth V, Syed HA, Evans J. Eczema. StatPearls Publishing; 2024. Accessed March 31, 2026. https://www.ncbi.nlm.nih.gov/books/NBK538209 Jatwani S, Hearth Holmes MP. Subacute cutaneous lupus erythematosus. StatPearls Publishing; 2024. Accessed March 31, 2026. https://www.ncbi.nlm.nih.gov/books/NBK554554 Thiboutot D, Anderson R, Cook-Bolden F, et al. Standard management options for rosacea: the 2019 update by the National Rosacea Society Expert Committee. J Am Acad Dermatol. 2020;82(6):1501-1510. doi:10.1016/j.jaad.2020.01.077 Ludmann P. 7 rosacea skin care tips dermatologists recommend. American Academy of Dermatology. Updated April 3, 2024. Accessed April 16, 2026. https://www.aad.org/public/diseases/rosacea/triggers/tips Sent from my iPhone Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574 Please excuse the shortness of this message, as it has been sent from a mobile device.

HS nd pregnancy

Managing Hidradenitis Suppurativa in Pregnancy Tori Rodriguez, MA, LPC | May 1, 2026 Significantly more women than men develop hidradenitis suppurativa (HS), with a majority of cases occurring among patients of reproductive age. 1 Pregnancy and the postpartum period presents additional challenges in the management of patients with HS due to associated adverse events and increased complexity of therapeutic regimens. Research exploring the relationship between HS, pregnancy, and the post-partum period has begun to gain momentum. Studies have emerged examining HS and associated maternal and fetal outcomes, guidelines were developed on treatments specific to pregnant and breastfeeding patients, and more attention has been given to patient desires for family planning than ever before. Recent Findings on Pregnancy Outcomes in HS Across numerous studies, HS has been linked to a range of adverse events in both pregnancy and childbirth. “Pregnant mothers with HS are at higher risk for hypertension, gestational diabetes, cesarean delivery, severe maternal morbidity, preterm birth, and birth defects compared with those without HS,” explained Chris Adigun, MD, founder of the Dermatology and Laser Center of Chapel Hill. 1 https://www.dermatologyadvisor.com/features/hidradenitis-supp903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:16 AM Page 1 of 6“ Given how common this condition is and the significant impact it has on pregnancy and neonatal outcomes, there is a need for further research and ” investigation. A population-based longitudinal study published in 2024 found an increased risk for the following outcomes among patients with HS compared with patients without HS: Severe maternal morbidity (risk ratio [RR], 1.38; 95% CI, 1.03-1.84); Hypertensive disorders of pregnancy (RR, 1.55; 95% CI, 1.29-1.87); Gestational diabetes (RR, 1.61; 95% CI, 1.40-1.85); and Long-term risk for hospitalization (RR, 2.29; 95% CI, 2.07-2.55). 1 Among birth outcomes, an increased risk for preterm birth (RR, 1.28; 95% CI, 1.07-1.53) and cesarean delivery (RR, 1.18; 95% CI, 1.07-1.30) were noted among patients with HS. The children of mothers with HS had an increased risk for birth defects (RR, 1.29; 95% CI, 1.07-1.56) and long-term risk for childhood hospitalization (RR, 1.31; 95% CI, 1.18- 1.45). 1 The odds of a spontaneous abortion (14%), ectopic pregnancy (73.2%), therapeutic abortion (52.9%), and stillbirth (76.2%) compared with a live birth were significantly greater in patients with HS, according to analyses of a 2025 retrospective study. 2 Retrospective studies published in 2022 also observed heightened risks in many of these maternal and obstetric outcomes. 3,4 “However, a limitation of these studies is the lack of data regarding whether pregnancy outcomes may be influenced by HS disease severity or whether a patient’s HS disease is well-controlled,” noted Jennifer Hsiao, MD, clinical associate professor of dermatology and director of the Hidradenitis Suppurativa Specialty Clinic at Keck Medicine of the University of Southern California. https://www.dermatologyadvisor.com/features/hidradenitis-supp903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:16 AM Page 2 of 6Regarding HS outcomes, studies have demonstrated that while 24% of patients with HS reported symptom improvement during pregnancy, 20% reported worsening symptoms in pregnancy and 60% reported postpartum disease flares. 5 In a large French study published in 2025, a substantial number of women with HS indicated impairment in multiple areas of sexual functioning, and more than one- third reported that they had hesitated or decided not to have a child because of their HS. 7 Recommendations on HS Treatment During Pregnancy Several papers have discussed clinical insights and treatment considerations for patients with HS who are pregnant or breastfeeding. 5,7-9 While some therapies have adequate literature available to support their use in pregnant and breastfeeding patients, other typical HS therapies are contraindicated, and others still need further exploration. “It is important for women with HS to know that HS can still be treated while they are planning pregnancy and also when they are pregnant,” Dr Hsiao emphasized. “In addition, many patients with HS may automatically self-discontinue all medications when they find out they are pregnant,” Dr Hsiao added, which underscores the need for patient education and counseling on this topic prior to pregnancy. Managing HS in pregnancy requires consideration of potential risks to both the patient and the fetus. “Topical options, like prescription clindamycin lotion or benzoyl peroxide washes at low concentrations, are considered safe and are often used as first-line therapy,” said Marisa Garshick, MD, dermatologist at MDCS Dermatology: Medical Dermatology & Cosmetic Surgery and clinical assistant professor of dermatology at Weill Cornell Medicine. 9 “If systemic treatment is required, antibiotics such as clindamycin or cephalexin are generally preferred, but tetracyclines like doxycycline should be avoided,” Dr Garshick continued. https://www.dermatologyadvisor.com/features/hidradenitis-supp903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:16 AM Page 3 of 6Systemic retinoids and most hormonal therapies are also contraindicated during pregnancy due to fetal risks, Dr Adigun added. 9 “In terms of biologic therapy for HS during pregnancy, tumor necrosis factor-alpha antagonists have the most data supporting their safety, but there is increasing data for interleukin-17 inhibitors,” Dr Hsiao stated. 9 “ Contributing to pregnancy exposure registries will help improve our understanding regarding safety of biologics in pregnancy.” “There is also emerging evidence that using metformin is both safe and efficacious for HS during pregnancy,” Dr Adigun said. 9 “Procedures for HS flares, including intralesional steroid injections and incision and drainage of abscesses, may still be performed, though it is generally recommended to hold off on large HS excisions during pregnancy, if possible,” according to Dr Hsiao. 9 Dr Garshick highlighted the need for a multidisciplinary approach in the treatment of pregnant and postpartum patients, which should include collaboration with obstetricians and maternal-fetal medicine colleagues as needed. Additionally, “Optimizing comorbidities such as smoking cessation and glucose control can improve outcomes both for pregnancy and HS.” Dr Garshick further noted the importance of planning ahead with patients for safe, effective therapies after delivery and during breastfeeding, given the high prevalence of postpartum flares. A small survey-based study found that 83% of women with HS had not received guidance from their physician regarding the potential impact of HS and HS therapies on pregnancy outcomes. 10 “Open and ongoing conversations with patients about their goals for family planning and disease management are essential so that treatments may be adjusted if needed,” Dr Garshick advised. Remaining Gaps https://www.dermatologyadvisor.com/features/hidradenitis-supp903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:16 AM Page 4 of 6To improve outcomes in this patient population, additional research and education are warranted. Dr Hsiao pointed to the need for prospective studies that include data on HS disease course, severity, and treatment patterns during pregnancy, as well as the influence of these factors on maternal and neonatal outcomes in patients with HS. “There is definitely a gap in evidence regarding both safety and efficacy of new therapies for HS in pregnant and lactating women,” Dr Adigun said. “Given how common this condition is and the significant impact it has on pregnancy and neonatal outcomes, there is a need for further research and investigation.” “ One of the biggest challenges is the limited data on how to best manage HS during pregnancy,” according to Dr Garshick. She also cited the need for increased education of both patients and providers and greater collaboration between clinicians. “Education is key, as many patients and even some providers may not be aware of how HS can impact pregnancy outcomes, so increasing awareness could help with earlier intervention and better counseling,” Dr Garshick said. “Ultimately, more collaboration between dermatology, obstetricians, and primary care clinicians would help ensure patients receive comprehensive care throughout pregnancy and beyond.” References: 1. 2. 3. Li K, Piguet V, Croitoru D, et al. Hidradenitis suppurativa and maternal and offspring outcomes. JAMA Dermatol . 2024;160(12):1297-1303. doi:10.1001/jamadermatol.2024.3584 Walsh DP. Pregnancy outcomes in hidradenitis suppurativa patients. AMIA Annu Symp Proc . 2025;2024:1169-1175. PMID:40417565 Fitzpatrick L, Hsiao J, Tannenbaum R, Strunk A, Garg A. Adverse pregnancy and maternal outcomes in women with hidradenitis suppurativa. J Am Acad Dermatol . 2022;86(1):46-54. doi:10.1016/j.jaad.2021.06.023 https://www.dermatologyadvisor.com/features/hidradenitis-supp903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True 28/5/26, 8:16 AM Page 5 of 64. 5. 6. 7. 8. 9. 10. Sakya SM, Hallan DR, Maczuga SA, Kirby JS. Outcomes of pregnancy and childbirth in women with hidradenitis suppurativa. J Am Acad Dermatol. 2022;86(1):61-67. doi:10.1016/j.jaad.2021.05.059 Seivright JR, Villa NM, Grogan T, et al. Impact of pregnancy on hidradenitis suppurativa disease course: a systematic review and meta-analysis. 2022;238(2):260-266. doi: 10.1159/000517283. Özbek L, Güldan M, Alpsoy E, Vural S. Hidradenitis suppurativa treatment during pregnancy and lactation: navigating challenges. Int J Dermatol. 2025;64(7):1173-1185. doi:10.1111/ijd.17672 Fite C, Taieb C, Nassif A, et al. High sexual impact of hidradenitis suppurativa in women with more than one-third of patients renouncing a desire for pregnancy: Results of a nationwide study in France. Clin Exp Dermatol. 2025;50(8):1647-1649. doi:10.1093/ced/llaf116 Chung CS, Park SE, Hsiao JL, Lee KH. A review of hidradenitis suppurativa in special populations: Considerations in children, pregnant and breastfeeding women, and the elderly. Dermatol Ther (Heidelb) . 2024;14(9):2407-2425. doi:10.1007/s13555-024-01249-2 Ghanshani R, Lee K, Crew AB, Shi VY, Hsiao JL. A guide to the management of hidradenitis suppurativa in pregnancy and lactation. Am J Clin Dermatol. 2025;26(3):345-360. doi:10.1007/s40257-025-00935-x Adelekun AA, Villa NM, Hsiao JL, Micheletti RG. Pregnancy in hidradenitis suppurativa – patient perspectives and practice gaps. JAMA Dermatol. 2021;157(2):227-229. doi:10.1001/jamadermatol.2020.5162 Sent from my iPhone Benjamin Hidalgo-Matlock Skin Care Physicians of Costa Rica Clinica Victoria en San Pedro: 4000-1054 Momentum Escazu: 2101-9574 Please excuse the shortness of this message, as it has been sent from a mobile device.

Finasteride dosis baja y disfunción eréctil... nueva data.

May 19, 2026

Low-dose finasteride linked to higher erectile dysfunction risk over time

WASHINGTON, DC -- May 19, 2026 -- A large retrospective study of more than 10,000 men with androgenetic alopecia found that low-dose finasteride (1 mg) was associated with a significantly increased risk of new-onset erectile dysfunction at both 1 year and 3 years compared with matched controls not taking the drug.

The findings, presented at the 2026 Annual Meeting of the American Urological Association (AUA), highlight the need for clinicians to discuss potential long-term sexual side effects with younger patients considering finasteride therapy and reinforce the importance of shared decision-making in hair loss treatment.

“Finasteride remains an effective, FDA-approved treatment, and for many men, the benefit to their hair and to their confidence will outweigh the risk that we observed,” reported Hriday Bhambhvani, Weill Cornell Medicine, New York, New York.

For the study, the researchers evaluated data from the TriNetX Research Network, identifying men aged 18 and 45 years with androgenetic alopecia and no prior history of erectile dysfunction. Using propensity score matching, 5,091 men who were prescribed 1 mg finasteride were compared with 5,091 controls, balancing groups for age, body mass index, race and ethnicity, depression, anxiety, tobacco use, alcohol use, hypertension, hyperlipidaemia, type 2 diabetes, and sleep apnoea.

For the primary outcome, no significant differences were observed between the 2 groups in terms of new-onset erectile dysfunction at 6 months (risk ratio [RR], 1.32; P = .21).

However, a significantly higher incidence of erectile dysfunction was observed with the finasteride group at 1 year (1.61% vs 0.96%; RR, 1.67; P = .004) and at 3 years (3.73% vs 2.36%; RR, 1.58; P = .0001).

“As we looked further out, a significant gap emerged at 3 years and those on finasteride had a meaningfully higher rate of erectile dysfunction, at about 4% compared to roughly 2.8% in the control group,” Bhambhvani said. “That corresponds to about a 46% higher risk. We also found significantly higher rates of low libido and ejaculatory dysfunction at the 3-year mark in the finasteride group.”

A further sensitivity analysis of the finasteride cohort compared with a separate propensity-matched cohort of men prescribed oral minoxidil 2.5 mg also similarly showed an increased 3-year risk for PDE5i prescription (4.03% vs 1.84%; RR, 2.19; P = .007). However, no difference in erectile dysfunction rates were observed at the 6-month and 1-year timepoints in the sensitivity analysis.

“The absolute difference in erectile dysfunction at three years was about 1.3%,” said Bhambhvani. “That means approximately 1 in 79 men on finasteride will develop erectile dysfunction as a result of the medication. Ultimately, the core message here is that shared decision-making providers should be having this conversation up front, laying out the real but modest risks discussing alternatives and letting the patient weigh in.”

“It's also worth noting that our study was not designed to assess whether these side effects persist after stopping finasteride,” he added. “That remains an important question for future research.”

[Presentation title: Risk of Erectile Dysfunction Among Reproductive-Aged Men Following Low-Dose Finasteride Use for Androgenetic Alopecia: A Propensity-Matched Cohort Study]

Prithviraj Bose, MD

EBAC® CE

Guias de manejo melanoma no operable 2026

A clinical practice guideline has been published that provides recommendations on the use of systemic therapy in patients with unresectable, metastatic cutaneous melanomas. These guidelines were published by Cancer Care Ontario.

The evidence-based recommendations apply to adults with unresectable nodal or distant metastatic cutaneous melanoma, defined as American Joint Committee on Cancer (AJCC) 8th edition stage IIIC/D or stage IV, who are candidates for systemic therapy. Intended users of the guideline include medical oncologists, dermatologists, and other clinicians involved in melanoma care. The recommendations reflect a decade-long therapeutic shift driven by immune checkpoint inhibitors — including anti-programmed cell death protein 1 (anti-PD-1) inhibitors, anti-cytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4) inhibitors, and anti-lymphocyte-activation gene 3 (anti-LAG-3) agents — and BRAF/MEK-targeted therapies.

First-Line Therapy: BRAF Wild-Type Disease

For patients with BRAF wild-type melanoma, recommended first-line options include nivolumab plus ipilimumab, nivolumab plus relatlimab, nivolumab monotherapy, and pembrolizumab monotherapy.

Nivolumab 1 mg/kg plus ipilimumab 3 mg/kg is to be administered intravenously once every 3 weeks for 4 total doses, followed by nivolumab 3 mg/kg every 4 weeks until progression, toxicity, or the need for other treatment considerations. Nivolumab 480 mg plus relatlimab 160 mg should be administered intravenously every 4 weeks until progression. Nivolumab monotherapy is to be administered intravenously in a dose of 3 mg/kg every 2 weeks or 6 mg/kg every 4 weeks, with either dose continued until progression, toxicity, or other considerations. Similarly, pembrolizumab is to be administered intravenously in a dose of 2 mg/kg every 3 weeks or 6 mg/kg every 4 weeks for a maximum of 2 years, with the potential for retreatment for 1 year.

Due to the evolving environment surrounding systematic therapy for unresectable, metastatic melanoma, indications and approvals are changing rapidly.

Evidence is anchored in a 2018 Cochrane review and multiple randomized controlled trials. Anti-PD-1 therapy (nivolumab or pembrolizumab) significantly improved overall survival (OS) and progression-free survival (PFS) compared with ipilimumab, with lower rates of grade 3-4 toxicity. Better PFS but higher rates of grade 3-4 treatment-related adverse events occurred with nivolumab combination therapy vs nivolumab monotherapy. Nivolumab plus relatlimab demonstrated improved PFS compared with nivolumab alone, with higher toxicity rates than nivolumab alone but lower than with nivolumab plus ipilimumab. While chemotherapy remains an option, immunotherapy is preferred due to superior survival outcomes.

First-Line Therapy: BRAF-Mutated Disease

For patients with BRAF-mutated melanoma, both immunotherapy and targeted therapy are recommended. In addition to the recommended treatment options for BRAF-wild type melanoma, patients with BRAF-mutated melanoma may also receive BRAF/MEK inhibitor combinations of dabrafenib plus trametinib, encorafenib plus binimetinib, or vemurafenib plus cobimetinib. However, immunotherapy is preferred as first-line treatment based on sequencing data.

Dosing for nivolumab plus relatlimab and nivolumab monotherapy are the same for patients with BRAF-mutated disease as patients with BRAF-wild type disease. Nivolumab plus ipilimumab is to be administered intravenously every 3 weeks for up to 4 doses, followed by nivolumab 6 mg/kg every 4 weeks until progression, toxicity, or other considerations. Pembrolizumab monotherapy is available intravenously for up to 2 years with a 1-year potential retreatment period in a dose of 2 mg/kg every 3 weeks, 4 mg/kg every 6 weeks, or 6 mg/kg every 4 weeks. Dabrafenib 150 mg should be taken twice daily and trametinib 2 mg should be taken once daily, both orally. Similarly, encorafenib 450 mg should be taken once daily while binimetinib 45 mg should be taken twice daily, both orally. Vemurafenib 960 mg should be taken twice daily with cobimetinib 60 mg once daily for 21 days with a 7-day rest period in each 28-day cycle.

Combination BRAF/MEK inhibitors vs BRAF monotherapy consistently demonstrated improved outcomes with a reduced mortality risk without increased toxicity in pooled analyses. Improved PFS and OS were observed with encorafenib plus binimetinib vs vemurafenib. Other trials similarly supported dabrafenib plus trametinib.

Triplet regimens (BRAF/MEK plus anti-PD-1/PD-L1) yielded mixed results. Some analyses demonstrated PFS improvements but triple-therapy regimens did not consistently improve OS and were associated with higher grade 3-4 toxicity than double-therapy regimens.

Sequencing trials provide key guidance. Superior 2-year OS and PFS were observed when patients received nivolumab plus ipilimumab first, followed by targeted therapy at progression. Sustained superiority of immunotherapy-first strategies was confirmed at 5 years. Initial immunotherapy, with or without short targeted therapy, was preferred over targeted therapy-first approaches. Continuous BRAF/MEK dosing was superior to intermittent dosing.

PD-1-Refractory Disease

For patients with BRAF wild-type melanoma who are refractory to PD-1 monotherapy (including both primary and acquired resistance), recommended options include nivolumab plus ipilimumab or pembrolizumab plus ipilimumab. Nivolumab plus ipilimumab improved PFS compared with ipilimumab alone.

For PD-1-refractory BRAF-mutant melanoma, options include combination immunotherapy with nivolumab plus ipilimumab, nivolumab plus relatlimab, or pembrolizumab plus ipilimumab, as well as BRAF/MEK inhibitors. Subgroup analyses showed PFS benefits for pembrolizumab in certain previously treated BRAF-mutant populations.

Dosing schedules for all regimens are consistent among patients who are and are not refractory to PD-1 monotherapy.

Molecular and Clinical Subtypes

For NRAS-mutant melanoma, binimetinib may be considered with or without immunotherapy. Binimetinib improved PFS compared with dacarbazine, although responses were modest.

For KIT-mutant melanoma, evidence is limited to single-arm studies. Due to low-quality evidence and absence of randomized controlled trials, no specific recommendation is made beyond following general systemic therapy guidance.

For brain metastases, nivolumab plus ipilimumab is recommended. In trials evaluating patients with asymptomatic brain metastases, greater rates of intracranial response were observed with combination therapy vs nivolumab alone. Combination immunotherapy was also favored over chemotherapy-based approaches based on 7-year OS data. Further, BRAF/MEK inhibitors demonstrated promising intracranial response rates in BRAF V600-mutant brain metastases, although responses were less durable than in extracranial disease. Radiation therapy, particularly stereotactic approaches, remains an important component of multidisciplinary care.

Implementation and Evidence Limitations

For all patients, clinical trial participation is encouraged when standard options fail or are not acceptable.

The guideline emphasizes shared decision-making, balancing OS/PFS benefits against toxicity, patient comorbidities, and preferences. Toxicity profiles vary significantly, particularly with combination immunotherapy.

Key limitations include the lack of direct head-to-head randomized controlled trial comparisons between immunotherapy and targeted therapy, limited predictive biomarkers beyond BRAF mutation status, and reliance on subgroup analyses for brain metastases and refractory populations. Heterogeneity across trials precluded meta-analysis. Cost-effectiveness was outside the scope of these recommendations.

Future Directions

Further biomarker-driven research is needed to personalize therapy, optimize sequencing, and refine treatment duration strategies. Ongoing trials in NRAS-mutant disease and novel combinations may further evolve the therapeutic landscape.

Overall, the guideline reflects a paradigm in which immunotherapy, particularly in blocking combination immune checkpoints, provides durable survival benefit and is generally favored as first-line therapy, with targeted therapy integrated strategically based on mutation status, disease progression, and clinical circumstances.

Guideline authors concluded, “Due to the evolving environment surrounding systematic therapy for unresectable, metastatic melanoma, indications and approvals are changing rapidly.”

References:

Petrella T, Kellett S, Knight G, et al; Melanoma Disease Site Group. Systemic treatments for unresectable and metastatic cutaneous melanoma. Cancer Care Ontario. Published January 5, 2026. Accessed February 17, 2026. https://www.cancercareontario.ca/en/guidelines-advice/types-of-cancer/79966

Lisa Kuhns, PhD

Lisa Kuhns, PhD is an experienced medical writer specializing in news-focused content for healthcare professionals. With over 15 years in the life sciences and 5 years of freelance experience, she brings a keen editorial eye and scientific rigor to the development of timely, clinically relevant news articles and summaries. Lisa also has extensive experience supporting accredited continuing medical education (CME), including the development of needs assessments and expert-driven slide decks across multiple therapeutic areas. Her work supports evidence-based clinical decision-making and bridges science and medicine to keep clinicians informed and engaged. Website: www.lgkmedicalwriting.com LinkedIn: https://www.linkedin.com/in/lisakuhns/

Espectro de Lesiones de Spitz

Exploring Spitz nevi in the molecular era

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Dermatopathologists discuss how to approach spitzoid lesions and how molecular testing can aid in assessing their potential malignancy.

Feature

By Allison Evans, Assistant Managing Editor, April 1, 2026

Spitz nevi. Spitz tumor. Spitz melanoma. It has long been recognized that the histopathologic differential diagnosis between a Spitz nevus and melanoma — and the spectrum in between — can be challenging, with hazards related to under- and overtreatment. The advent of advanced molecular techniques like next generation sequencing (NGS), conventional or microarray comparative genomic hybridization (CGH), and fluorescence in situ hybridization (FISH), have provided new sophisticated tools to assist with this vexing differential diagnosis. 

Spitz nevus is named after Sophie Spitz, a pathologist who reported a case series of “melanomas of childhood” in 1948. Nearly all of Spitz’s original series of 13 cases are now regarded as representing Spitz nevi, with only one case having proved to be a melanoma resulting in metastasis and death. 

“This case series fundamentally changed our understanding of these lesions,” said Alina Bridges, DO, FAAD, director of cutaneous pathology at Northwell Health and director of dermatopathology at the Zucker School of Medicine at Hofstra/Northwell. 

Spitz refers to a family of melanocytic tumors that have commonalities, which include certain morphologic features under a microscope but also common genomic features, said Pedram Gerami, MD, FAAD, IDP Foundation professor of skin cancer research and professor of dermatology and dermatopathology, pathology, and pediatrics at Northwestern’s Feinberg School of Medicine.

“In 2013, the primary genomic drivers of Spitz were discovered,” he explained, “which allowed us to use genomics to more objectively and definitively determine if a lesion belongs to the Spitz family and to exclude mimickers of Spitz when the genomics do not match a Spitz profile.” 

To biopsy or not

According to Dr. Gerami, it is not necessary to biopsy all Spitz nevi. “However, prior to the biopsy, we don’t always know if we are dealing with a lesion in the Spitz family or a mimicker of Spitz. If the lesion is in the Spitz family we may not necessarily know if we are dealing with a Spitz nevus, atypical Spitz nevus, Spitz tumor (also called a melanocytoma), or Spitz melanoma.”

It’s a matter of risk management, he continued. “If you imagine the Spitz spectrum from Spitz nevus to atypical Spitz nevus to Spitz tumor to Spitz melanoma, in a prepubertal child the probability of being toward the benign end of this spectrum is significantly higher. In prepubertal children with symmetric macular lesions or even symmetric small papular lesions, observation is completely acceptable.” 

“Biopsies should be done any time the lesion exhibits atypical features such as a larger lesion — greater than 1 cm — exhibiting rapid growth or is ulcerating, if there’s any asymmetry, or if you have a patient who is older or post-pubertal,” Dr. Bridges said. 

In the ages between puberty and 40, the decision to biopsy is often made on a case-by-case basis, Dr. Gerami noted. “In a patient older than 40, the probability of malignancy in a lesion with a clinically spitzoid appearance becomes significant enough that I typically would biopsy these. The greatest threat is not a malignant Spitz melanoma but rather a conventional malignant melanoma mimicking a Spitz.”

“If the pigmented lesion in a child is a classic fit for a Spitz nevus, including the dermoscopy findings and the clinical evolution, then it can be safely monitored,” agreed Jeffrey North, MD, FAAD, professor of dermatology and pathology and managing director of UCSF Dermatopathology and Oral Pathology Service. 

“But it really needs to match all of those characteristics — symmetrical appearance, well circumscribed, no rapid growth, a uniform starburst pattern or globular pattern on dermoscopy.” He also noted the importance of ensuring the patient has the means to reliably follow up so the lesion can be monitored if a biopsy is not done.

Advances in dermatopathology

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Learn more about the latest trends and developments in dermpath.

Excision

According to the National Comprehensive Cancer Network (NCCN) Guidelines, the lesion should be removed in its entirety, Dr. Bridges said. “Dermatologists should do an excisional or complete biopsy, whether or not that’s a deep shave, a punch biopsy for smaller lesions, or an elliptical excision so that you can get around it with 1- to 3-millimeter margins.”

The ability to do molecular testing is mostly dependent on having adequate tumor DNA, Dr. Gerami agreed. “This can be compromised by doing small shaves of small lesions or small biopsies of large lesions, resulting in inadequate sampling. Regardless of the biopsy method, if the entire lesion is removed, this maximizes the likelihood that there will be enough tissue for immunostains and molecular testing.” 

“If I have just a small piece of tissue, then I have to sacrifice the number of immunostains that I’m going to do so that I have enough tissue left to do the molecular testing,” Dr. Bridges added.

This is particularly important when it comes to pediatric patients, she continued. “The parent and the child may not be too happy with you saying that you need to perform another excision to get a larger sample when we should have done it in the first place.”

Dr. North explained that he frequently sees Spitz tumors biopsied where they’re transected across the base, and oftentimes at the edges, and that really limits what the dermatopathologist can do in assessing the neoplasm. 

“We may be able to do molecular testing, but we can’t see if there’s good dermal maturation, if the lesion is well circumscribed — we can’t see what the bottom of the tumor looks like. Sometimes, a Spitz tumor may have an atypical part that’s not visible in the superficial part,” he added.

Diagnosing Spitz lesions: Case examples

Dr. Bridges highlighted one of her cases in which she received a specimen to rule out a dermatofibroma. “It may be challenging to clinically suspect Spitz nevi because they may not be pigmented. With immunostains and molecular testing, I rendered a diagnosis of Spitz melanoma as opposed to severely atypical Spitz nevus.”

“You can’t tell based solely on histomorphology, and I only did a few immunostains because I had very little tissue. I tried to see if there was any mitotic activity — there wasn’t. I sent this for a chromosomal microarray (similar to comparative genomic hybridization), which identified four copy number alterations; anything greater than three is considered suspicious for melanoma.”

In another of Dr. Bridge’s cases, a teenager presented with a history of a lesion on the ear. A superficial shave biopsy was performed, and it was diagnosed as a Spitz nevus. The lesion recurred and a deeper shave biopsy was performed. “The lesion was very atypical; it had three mitoses and was diagnosed as a Spitz melanoma based on the immunostains.”

“The first workup that was done came from haemotoxylin and eosin (H&E) and the second one came from immunostains. When I got the case, I did molecular testing and was able to downgrade the lesion to a severely atypical Spitz tumor rather than a Spitz melanoma,” she added.

Exploring Spitz: A spectrum of Spitz melanocytic lesions

Spitz nevi - Definitively benign

Atypical Spitz nevi - Definitively benign but with atypical histologic features

Spitz tumors - Borderline morphologic features but with most cases having an indolent clinical course

Spitz melanoma - Malignant melanoma version of a Spitz

Molecular diagnostics

Advances in molecular techniques have revealed many genetic differences between benign nevi and melanomas. Next generation sequencing, chromosomal microarray and/or CGH, and FISH are all tests that can be useful in certain scenarios to assess Spitz neoplasms and determine where they lie on the Spitz spectrum.

“Over the years that I’ve practiced, I have a lot more satisfaction handling these lesions,” Dr. Bridges said. “Before it was very ambiguous. You could say that it’s benign or atypical, but you couldn’t definitively rule out malignancy. We used to use the phrase ‘uncertain malignant potential’ all the time for these lesions, but now because of advanced immunostains and molecular testing, I can not only diagnose, but I’m almost prognosticating as well.”

The most important thing to determine is whether you are really dealing with a Spitz or a Spitz mimicker, Dr. Gerami emphasized. “Melanocytic tumors with mutations in BRAF, NRAS, GNAQ, and GNA11, for example, are immediately excluded from the Spitz family and belong to other classes of melanocytic neoplasia. However, an HRAS mutation or a characteristic Spitz fusion is highly consistent with classification in the Spitz family.” 

Immunostains

One of the most important stains is BRAF because all Spitz lesions will be negative for BRAF, Dr. Bridges said. “Conventional nevi usually have a single driver mutation — most commonly BRAF and less frequently NRAS.”

Dr. Bridges also uses the p16 stain to determine whether that tumor suppressor has been disabled. “In order to determine whether the specific mutation (CDKN 2A/2B genes) associated with melanoma is found, we need to do further molecular testing.”

While PRAME can be used, it has pitfalls because melanomas can be PRAME positive or negative, and benign lesions can be PRAME positive. Dr. Bridges recalled her aforementioned case of the teenager with the ear lesion that was downgraded from a Spitz melanoma to a severely atypical Spitz tumor. “She was diagnosed with Spitz melanoma because her p16 was lost and her PRAME was positive.”

Immunostains can be helpful, noted Dr. North. “Some can identify mutations that would exclude a Spitz family tumor. However, immunostaining to confirm a Spitz family tumor is limited. ALK staining to detect an ALK gene fusion in the Spitz family is the most reliable. The remaining immunostains for Spitz genetic drivers (e.g., NTRK1, ROS1, etc.) can be challenging to interpret and can lead to misdiagnosis. Most pathologists try immunostains before molecular testing.”

You can’t interpret any of these tests in isolation, Dr. Bridges remarked. “If there is severe atypia or if we’re in the category of Spitz tumors or melanocytomas and they have mitoses, then we’re going to be doing next generation sequencing to classify the lesion.” 

NGS and CGH

Comparative genomic hybridization can be helpful by providing the chromosomal copy number information and, in some cases, can show features suggestive of a Spitz gene fusion, but it’s not as comprehensive as NGS. “We rarely do CGH now because our next generation sequencing panel gives us the same data,” said Dr. North. “It provides mutation and fusion information about whether the tumor has a Spitz family genetic driver as well as potential additional progression mutations in other oncogenes and tumor suppressor genes. It also provides chromosomal copy number information similar to CGH to give a comprehensive genetic analysis of the tumor.”

Next generation sequencing identifies the specific driver alteration, so it definitively classifies the lesions, Dr. Bridges said. “Classification is important because even atypical Spitz tumors have an excellent long-term prognosis, despite having worrisome histologic or immunohistochemical features. There have been very large studies that showed event-free survival of 98% and overall survival of 100%.”

Spitz melanomas typically have additional pathogenic mutations, such as a TERT promoter mutation, and copy number aberrations, Dr. Bridges said.

NGS helps dermatopathologists classify the melanocytic pathway, Dr. North said. “This becomes really important because when you look at them under a microscope, they may look like a Spitz family tumor. But when you sequence them, they may not have the genetics of a Spitz tumor.”

“If there isn’t truly a Spitz genetic driver — if instead there is a BRAF mutation — that’s potentially a worse prognosis in an atypical tumor with spitzoid features. For the most part, even these very atypical Spitz tumors tend not to behave as aggressively. You can often only get this type of information with next generation sequencing,” he added.

PRAME sets its eyes on the road to fame

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Jason B. Lee, MD, FAAD, discusses preferentially expressed antigen in melanoma (PRAME) in evaluating melanocytic neoplasms.

FISH

There is a middle ground if there isn’t enough tissue, Dr. Bridges noted. “You could use FISH to detect chromosomal aberrations, which requires less tissue and has quicker turnaround time. However, 20% of melanomas will be FISH negative.” 

FISH is one of the oldest molecular tests used to assess Spitz tumors, said Dr. North. “Because it has the most studies published on it, it tends to be what’s most readily approved by insurance. With FISH you’re only able to look at four to eight segments of the genome, while NGS looks at a large amount of the genome with targeted panels looking at 300-600 of the most mutated genes in cancer.”

“We often see consults where physicians send specimens because the tumor looks very atypical. There may be loss of p16 expression and PRAME positivity, so it looks quite worrisome for a melanoma,” said Dr. North. “But in a 10-year-old child, you don’t want to make a melanoma diagnosis without having a full assessment of the tumor. We would get NGS on this, and sometimes it ends up being on the benign side even with the concerning features noticed in the initial workup.”

Sometimes more than one test is indicated, Dr. Gerami said. “NGS may be performed to identify the primary driver and some progression events. If the pathologist does not find anything and is still worried, then CGH or FISH may be added to look for other potential progression events.”

Next steps

With severely atypical Spitz tumors, dermatologists often want to know whether they should do a sentinel lymph node biopsy, Dr. Bridges said. “There’s no reason to do a sentinel lymph node biopsy because it has no prognostic benefit. Yes, they can have a positive sentinel lymph node biopsy, but it doesn’t predict a poor outcome in these patients, particularly pediatric patients.”

Everybody wants to know about margins, said Dr. Bridges. “If it’s anything that is atypical or severely atypical, then you have to excise it with 5-millimeter margins; you treat Spitz melanomas like any other melanoma.”

If a dermatologist receives a report in which NGS is done, if anything is not clear, call the dermatopathologist, advised Dr. North. “It’s not the same as a lab test in which there is a clear positive or negative result.” 

“It’s very easy to get confused when seeing all the next generation sequencing data. It can even confuse the molecular pathologists sometimes because there may be mutations listed in the reports that are not significant,” he continued.

“If you feel like there’s a disconnect between your clinical impression and the report, you should call the dermatopathologist to walk through everything and ask questions about whether the mutations are significant,” said Dr. North. “Don’t feel you like you have to have a grasp of everything molecular to make the call.”

“Perhaps there was not a definitive diagnosis in a biopsy without comprehensive testing,” continued Dr. North. “The call could simply be, ‘Could we do some additional testing to see if we could get a more definitive diagnosis?’ or ‘Could we get a second opinion consult with possible additional testing?’”

Dr. Gerami urges dermatologists to forge a good working relationship with their dermatopathologist and discuss cases that are concerning. “If the diagnosis is straightforward from the pathologist, then some of these molecular tests may not be needed. If they are needed, then it may be worthwhile to discuss the details of the case with the pathologist to understand the testing and what level of certainty the pathologist has of a benign or malignant diagnosis.”

Spitz pathology reports can be anxiety-inducing because of how atypical and yet how clinically unaggressive they can be, Dr. North said. “The goal should be proper treatment, not overtreatment, in these tumors that generally have a very excellent prognosis, even in that intermediate category of an atypical Spitz tumor.” 

https://www.intramed.net/content/como-leer-y-comprender-un-articulo-cientifico

¿Cómo leer y comprender un artículo científico?

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Uno de los principales pilares de la práctica médica es la investigación. Y para mejorar como profesionales, tenemos que saber cómo leer e interpretar una publicación científica.

Antes de comenzar con la lectura de un artículo, tenemos que conocer la variedad de evidencia científica que hay. Entonces:

¿Qué tipos de artículos existen? ¿Y cuáles son sus beneficios?

· Artículo original: investigaciones directas para evaluar conclusiones rescatadas del contacto con poblaciones estadísticamente relevantes.

· Reportes: pueden ser "reportes breves", que tienen el mismo objetivo y contenido que los artículos originales, pero redactados de forma resumida; o también pueden ser "reportes de casos", que buscan compartir eventos aislados relevantes.

· Artículos de revisión: publicaciones con la mayor evidencia científica y el menor sesgo. Aquí se incluyen las revisiones sistemáticas, los metanálisis y las guías (que funcionan como directrices).

· Revisiones narrativas: los autores redactan sobre su área de expertise, creando una mezcla entre evidencia y práctica personal.

· Artículos de opinión: redacción desde lo empírico (no siempre fundamentado).

· Cartas al editor: respuestas de otros profesionistas ante artículos publicados para contrastar sus conclusiones basándose en otros hallazgos.

Lo primero es únicamente "ver" el título y el abstract del artículo que deseamos evaluar, es decir, por el momento no vamos a profundizar en ninguno de estos apartados. Esto, para que podamos generar nuestra propia impresión del texto sin dejarnos llevar por los primeros resúmenes que los autores nos proponen. Para comenzar formalmente con la lectura a conciencia, el Dr. Oscar Arias nos recomienda iniciar con la introducción. Este apartado nos servirá para conocer y empaparnos del panorama que se conoce acerca del tema a evaluar; esta sección nos otorgará los antecedentes, la pregunta de investigación, y nos deja echar un vistazo a cómo los autores buscarán llenar el vacío en el conocimiento propuesto una vez que este trabajo se finalice.

Posteriormente, la recomendación es acudir a la sección de resultados e inclusive buscar las figuras y tablas expresadas. Aquí nos ilustrarán de forma esquemática el diseño del estudio, la cronología, los datos estadísticos y lo mas relevante: una simplificación de los hallazgos (que, en muchas ocasiones, cuando los manuscritos son de muy buena calidad, nos pueden otorgar gran parte de la información que necesitamos saber). Específicamente, en esta sección de "resultados", lo ideal es comenzar por la evaluación de las tablas y figuras y después dar lectura al texto redactado en este mismo apartado; la finalidad de seguir este método es formar un pensamiento crítico antes de leer lo que los autores busquen hacernos entender. Además, nos sirve para identificar cualquier irregularidad que se pudo haber producido durante la elaboración del trabajo.

Una vez que hayamos concluido con este apartado, continuaremos con la discusión y la conclusión. Aquí se nos presentará un breve resumen de la introducción (para darnos un "antes de este estudio"), otro resumen de los resultados (para darnos un "durante") e incluso también se contrastarán estos con diversos hallazgos en otros manuscritos de distintos autores sobre la misma materia a tratar (este contraste nos otorgará un "después de este estudio"). En este punto, es importante que mantengamos ese pensamiento crítico con el que comenzamos a leer el trabajo para evitar únicamente guiarnos por lo que los autores nos quieren hacer entender con el "después de este estudio"; el propósito de este pensamiento crítico es evitar (en caso de que suceda) quedarnos con un sesgo que se puede presentar en la conclusión de los autores.

En caso de que aún nos queden dudas o inquietudes en este punto, nos acercaremos al apartado de materiales y métodos, para evaluar cuál fue la verdadera estrategia creada por los autores para llegar a dichos resultados.

Continuaremos ahora con una evaluación personal. En otras palabras, tras la lectura en este orden, buscaremos identificar cuáles son nuestras conclusiones personales. Esto, para evaluar si el trabajo tiene la evidencia suficiente y nos sirve para responder la pregunta que en primera instancia nos hizo acercarnos a este manuscrito en específico.

Casi para terminar, acudiremos a las referencias utilizadas; principalmente, buscaremos las que contradigan el trabajo que recién evaluamos, para que, de forma personal, podamos contrastar ambos estudios y evaluar qué generó dicho cambio y, a su vez, si este cambio es válido.

Finalmente, regresaremos a los apartados del título y abstract para ponderar si los autores plasmaron de forma correcta el trabajo realizado. Llegado este punto, nos puede servir como herramienta el realizar un resumen sobre lo que entendimos de la lectura, para, como bien lo menciono, continuar con el pensamiento crítico.

Tener el conocimiento de la mejor evidencia actualizada, pero sin dejar de lado los conocimientos esenciales, los "artículos clásicos", pues gracias a estos podemos entender todo lo que hoy en día innova a la medicina.

Nos sirven para comprender, de forma contextualizada, el porqué de distintos escenarios en el área de la salud.

Ya para finalizar, el Dr. Oscar Arias nos comparte, a través de un artículo de su autoría, publicado en la revista npj Parkinson's Disease del portafolio de Nature, un ejemplo más extenso sobre cómo leer e interpretar un artículo médico.

A continuación, y aclarando lo anteriormente mencionado, una descripción gráfica y simplificada sobre cómo leer y obtener la mejor información de un artículo científico:

---

Especial agradecimiento al Dr. Oscar Arias por su apoyo y colaboración en la realización de esta columna.

Sent from my iPhone

Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

Please excuse the shortness of this message, as it has been sent from
a mobile device.

Skin Microbiome Medicine for Dermatology - Dermatology Advisor

https://www.dermatologyadvisor.com/features/skin-microbiome-medicine/?utm_source=eloqua&utm_medium=email&utm_campaign=NWLTR_DER_UPDT_SS-LIC-LAS-PP-10205_SL_022426_AF-thisone&hmemail=arj%2Fdu47fH0tIG%2BOxiMnyzIZDo7e%2Fi8h&sha256email=818ca2c110aeb8c0905b76eae9c8cf13eeedcf69cfe6587b8903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True

Breakthroughs in Skin Microbiome Medicine May Transform Dermatology

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Bryant Furlow

February 23, 2026

Human skin harbors complex microbial communities of bacteria, viruses, and fungi. A growing body of research shows that shifts in the species composition, diversity, and metabolic products of the skin ecosystem can open the door to invasion by harmful microbes, inflammatory responses, skin barrier dysfunction, and dermatologic disease.

"We have a complex relationship with our skin microbes, which are integral to immune homeostasis and repair, as well as mediators of local and systemic inflammation," explained Nathan Archer, PhD, assistant professor of dermatology at Johns Hopkins University School of Medicine.

The clinical implications of utilizing the skin microbiome in the treatment of dermatologic diseases could be profound.

Shifts in microbial community structure — especially reduced overall species diversity and the resulting predominance of pathogenic and pro-inflammatory species — precede the onset or worsening of symptoms in atopic dermatitis, eczema, acne, and psoriasis.^1-5 Large-scale genomic sequencing has identified previously unsuspected bacterial communities and microbial signatures that can help distinguish lesional skin from healthy skin, pointing toward new diagnostic and therapeutic targets.^1,5-7

Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair.

Recent research has also demonstrated that disruptions of skin ecology, called dysbiosis, are more consistently associated with acne and other inflammatory dermatoses than the overgrowth of Cutibacterium acnes or Staphylococcus aureus. Dysbiosis contributes directly to disease flares, challenging longstanding assumptions about the etiology of dermatologic diseases.^4,8,9 Indeed, dysbiosis appears to be a hallmark mechanism in inflammatory dermatoses like eczema, rosacea, and psoriasis, driven by altered microbiome-immune system interactions.⁸

Scientists are exploring how ecological engineering of the skin microbiome might offer alternatives to current therapies like antibiotics, which eradicate both pathogens and beneficial microbes and may worsen dysbiosis and induce treatment resistance.^10,11

"Understanding their roles opens the door to entirely new therapeutic paradigms: instead of only suppressing inflammation, we can begin to restore balance between our skin and the microbial community," Dr Archer said.

For example, preclinical research suggests that applying commensal bacteria can improve the integrity of the skin barrier and reduce S aureus overgrowth in atopic dermatitis.^10,12 Researchers are also investigating prebiotics, strain-specific probiotics, live bacteriotherapies, genetically engineered bacteriophages, and targeted phage cocktails for selectively culling pathogens from skin ecosystems.^7,10,11,13    

The field of microbiome dermatology is young and not without significant challenges, including the need for better standardization of research methodologies and further expansion of research ventures.^4,5 Yet experts maintain optimism about knowledge gained thus far and that these challenges will be overcome. They anticipate a clinical paradigm shift toward precision microbiome medicine in the years ahead.

The Skin Microbiome Beyond the Skin

The skin's microbial ecosystem includes a dermal microbiome beneath the skin's surface and a distinct epidermal microbiome interfacing the external environment, shaped by infants' early encounters with microbes, explained Richard Gallo, MD, PhD, professor and chair of the department of dermatology at the University of California San Diego School of Medicine. Intriguingly, Dr Gallo and his colleagues found that these microbial communities communicate with the microbiomes of other organ systems, like the gut.^14,15

Skin wounds affect intestinal bacteria, for example.¹⁶ "Our work discovered that injury or inflammation of the skin causes release of 'danger signals' that are detected by cells in the intestine," Dr Gallo said. "These cells then respond by producing antimicrobials that inappropriately kill some of the bacteria in the gut that help maintain gut health. This is important as it provides an explanation for the frequent co-occurrence of diseases of the skin and gut, and emphasizes the need to treat the whole patient, not just a single organ."

This skin-to-gut axis is not the only connection between skin and other microbiomes, Dr Gallo was quick to point out. "Important communication occurs between skin and lung, skin and brain, and skin and the cardiovascular system," he explained. "With continued work, we see important general medical breakthroughs coming from understanding these communication networks."

Indeed, a recent study showed that S aureus skin exposure can exacerbate lung inflammation, helping to explain the atopic march from atopic dermatitis to respiratory disease.¹⁷

"Clinically, this highlights the importance of early intervention in atopic dermatitis — addressing microbial dysbiosis and interleukin (IL)-36-driven inflammation before diseases of the atopic march develop, such as asthma," said Dr Archer.

For patients with overlapping atopic dermatitis and neutrophilic asthma, that finding bolsters the case for a more integrated clinical approach to achieve better outcomes, Dr Archer added. "Rather than treating skin and airway disease in isolation, clinicians might consider shared immunological pathways as therapeutic targets or agents that modulate or restore healthy microbial balance that could, in principle, benefit both skin and lung inflammation," he said.

Biomarkers like IL-36 and neutrophil signatures might be helpful for risk assessment and early therapeutic escalation in patients with atopic dermatitis, to prevent neutrophilic asthma progression, Dr Archer added.

"Elevated systemic IL-36 and neutrophil signatures could identify patients whose atopic dermatitis may be leading towards neutrophilic asthma or T2-low asthma, which is more treatment-resistant than T2-high asthma," he explained. "In fact, circulating IL-36 has already been associated with severe asthma in patients."

With his coauthors, Dr Archer also reported that bacteria like S aureus can promote skin regeneration through IL-1β-dependent signaling pathways, with important implications for wound care.¹⁸

"This suggests that indiscriminate topical antibiotic use may disrupt beneficial microbe-host interactions that aid healing," Dr Archer explained. "Microbiome-aware wound care that balances pathogen control with preservation of beneficial microbes may improve regenerative outcomes."

Atopic dermatitis and asthma are heterogeneous conditions with immunological subtypes, Dr Archer pointed out, and better understanding of their mechanistic underpinnings will enable the development of more personalized treatment approaches.

"Understanding which cytokine and microbial pathways drive an individual's disease — whether it be IL-36–neutrophil, Th2, or S aureus — may enable personalized therapy selection and better prediction of comorbidities like asthma or food allergy," Dr Archer said. "We are moving away from a one-size-fits-all mentality and entering an era of precision dermatology. Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair."

Are Skin Diseases Industrial Comorbidities?

In addition to genomics and molecular mechanism studies, insights into healthy skin microbiomes are being gleaned from cross-cultural research.

"Over the last few decades we've seen a steady rise in chronic inflammatory skin conditions, especially in Western countries and in places rapidly adopting Western lifestyles," explained study coauthor Julia Durack, PhD, Executive Director of the Holobiont Medical Research Foundation. "These diseases are much less common in traditional, non-industrialized communities. Because the skin microbiome is closely tied to skin health, we wanted to study the Yanomami, one of the last remaining hunter-gatherer groups, who rarely experience these conditions. By looking at their skin microbiome, we hoped to better understand what might be missing in modern populations and how that relates to the rise in skin disorders."

What they found was that the skin of this group who reside in the remote Amazonian rainforest share some bacterial communities with Western-nation populations, but with markedly greater species diversity (R² =.455; P =.001).¹⁹ A total of 115 previously unknown bacterial genomes were identified as part of the skin microbiome of these individuals.

"The Yanomami community we worked with has had very limited contact with outsiders, so it's unlikely that the shared taxa we observed were introduced by westerners. Instead, these are what we would call conserved microbial groups — taxa that are commonly found across humans and even other mammals," Dr Durack said. "What was particularly interesting in our data was that while the Yanomami share some of these same microbial groups with Western populations, the diversity within those groups was much greater. For example, their skin harbored a wider range of Staphylococcus species, including ones we didn't detect at all on Western skin. That suggests their microbiomes are not only intact but also more complex, reflecting a deeper ecological richness rather than acquisition from outside contact."

That wasn't just a reflection of the Yanomami people living in the species-rich tropics, where there are more bacterial and fungal species in general, Dr Durack said.

"People living traditional lifestyles tend to have more species-diverse skin microbiomes, and this is consistent across non-industrialized groups worldwide, not only those in the tropics," she explained. "The key factor appears to be lifestyle rather than geography. In industrialized societies, our skin microbiomes are less diverse and compositionally distinct, shaped by constant exposure to chemicals, pollution, antibiotics, and a lack of contact with beneficial microbes from soil, plants, and other natural environments."

Dr Durack and other researchers refer to conditions like acne, rosacea, psoriasis, and atopic dermatitis as industrialized comorbidities, meaning they are strongly linked to the ecological and microbial shifts that come with modernization and not something inherent to genetics or ancestry, she said.

For example, other researchers found that when urban children in Finland have more natural play areas, their skin microbiome's species diversity grows within a few weeks, along with measurable changes in immune regulation markers.²⁰

"This suggests that reintroducing environmental microbial exposures can directly influence health," Dr Durack said. "Our study extends this idea by showing that the Yanomami's continuous exposure to diverse environmental microbes likely helps maintain a complex skin microbiome. That complexity may be protective and its loss in industrialized societies could help explain the rise in inflammatory skin conditions we now consider hallmarks of modern living. Restoring microbial diversity on the skin could be an important way to boost resilience against inflammatory conditions."

The skin microbiome of a westernized adult who temporarily lived with the Yanomami shifted to Yanomami-like microbiomes, Dr Durack said, though it was lost upon their return to an industrialized setting.¹⁹

"That tells us it's not a closed door. Our skin microbiomes can adapt," she said. "In industrialized societies, we've largely lost this co-evolved relationship with our environment. While it may not be realistic to completely rewild our skin microbiomes to an ancestral state, Western medicine could take a more ecological approach: finding ways to reintroduce or support the right kinds of microbial exposures that strengthen the skin barrier and immune balance. This could open new avenues for preventive and therapeutic strategies in dermatology."

Challenges and Furthering the Research

Not surprisingly for an emerging field of knowledge, researchers caution that mechanistic uncertainties and gaps in methodological standardization must be addressed to strengthen preclinical research, and that large, well-designed, standardized clinical studies are needed to more clearly establish causality between the microbiomes and disease.^21,22

Early work with targeted bacteriophage culling has been promising so far, but little is yet known about long-term effects on commensal species, the potential for evolved resistance to phages, or off-target effects on beneficial microbes.¹³

Nor do we yet know the best strategies for ecological engraftment (defined as sustained integration of introduced species into the skin microbiome) or how species diversity and composition might affect resistance to introduced species.⁷

Yet direct-to-consumer marketing hype has gotten well ahead of the science, Dr Gallo cautioned. "An unfortunate lack of scientific rigor has occurred that has led to false claims and unrealistic expectations," he said. "The field is working through this, but several products are still sold without good scientific evidence that they are effective."

The field has taken its first tentative steps, but has yet to find its stride. "We still need to define how specific microbes and their products shape skin and systemic immunity, and when dysbiosis becomes pathologic," Dr Archer said. "This includes microbe-neuro-immune interactions, which are only beginning to be uncovered in the skin with much to be discovered about how skin microbes may affect distal neural development."

We also don't yet understand what nutrients skin microbes use, or how exactly transitions between homeostatic and inflammatory states might cause metabolic shifts in the microbiome, he noted.

"Longitudinal, mechanistic, and multi-tissue studies will be essential to close these gaps," Dr Archer said. "We are currently investigating how pathogenic bacteria gain a foothold onto our skin and why certain pathogens are commonly prevalent among multiple inflammatory skin conditions.If we can understand the strategies by pathogens to live on our skin, we hope to prevent colonization and exacerbation of inflammatory skin disorders that involve dysbiosis."

"We're only just beginning to understand how important the skin microbiome is for our overall health," agreed Dr Durack. "Most of what we know so far is based on studies of people in industrialized societies, which gives us a very narrow view. By broadening research to include communities with diverse ethnicities, lifestyles, and environments, we can uncover much more relevant insights into what truly supports healthy skin — and how modern lifestyles may be limiting that potential."

Disclosure: Weiss Biosciences Inc. funded the Yanomami skin microbiome study and paid Dr Durack's salary. Dr Nathan Archer has received previous grant support from Pfizer and Boehringer Ingelheim and was a paid consultant for Janssen Pharmaceuticals and Alphyn Biologics. Dr Gallo had no relevant disclosures.

References:

1. Chaudhary PP, Myles IA, Zeldin J, et al. Shotgun metagenomic sequencing on skin microbiome indicates dysbiosis exists prior to the onset of atopic dermatitis. Allergy. 2024;78(10):2724-2731. doi:10.1111/all.15806
2. Kim HB, Alexander H, Um JY, et al. Skin microbiome dynamics in atopic dermatitis: understanding host-microbiome interactions. Allergy Asthma Immunol Res. 2025;17(2):165-180. doi:10.4168/aair.2025.17.2.165
3. Asees A, Sadur A, Choudhary S. The skin microbiome in rosacea: mechanisms, gut-skin interactions, and therapeutic implications. Cutis. 2025;116(1):20-23. doi:10.12788/cutis/1240
4. Niedzwiedzka A, Micallef MP, Biazzo M, Podrini C. The role of the skin microbiome in acne: challenges and therapeutic opportunities. Int J Mol Sci. 2024;25(21):11422. doi:10.3390/ijms.252111422
5. Ruuskanen MO, Vats D, Potbhare R, et al. Towards standardized and reproducible research in skin microbiomes. Environ Microbiol. 2022;24(9):3840-3860. doi:10.1111/1462-2920.15945
6. Li Chengchen, Ravikrishnan A, Wijaya I, et al. Large-scale skin metagenomics reveals extensive prevalence, coordination, and functional adaptation of skin microbiome dermotypes across body sites. bioRxiv. Published online ahead of print June 8, 2025. doi:10.1101/2025.04.24.650393
7. Oh J, Voigt AY. The human skin microbiome: from metagenomes to therapeutics. Nat Rev Microbiol. Published online August 4, 2025. doi:10.1038/s41579-025-01211-9
8. Wilkhoo HS, Islam AW, Hussain S, Kadam SR, Rao ZK, Singh B. Skin microbiome and inflammatory dermatoses: a focused review. Costmoderma. 2025;5:107. doi:10.25259/CSDM_99_2025
9. Huang C, Zhuo F, Han B, et al. The updates and implications of cutaneous microbiota in acne. Cell Biosci. 2023;13:113. doi:10.1186/s13578-023-01072-w
10. Lyu Y, Shen J, Che Y, Dai L. Skin microbiome engineering: challenges and opportunities in skin disease treatment. iMetaOmics. 2025;2:e70012. doi:10.1002/imo2.70012
11. Ito Y, Amagai M. Controlling skin microbiome as a new bacteriotherapy for inflammatory skin diseases. Inflamm Regen. 2022;42:26. doi:10.1186/s41232-022-00212-y
12. Uberoi A, Murga-Garrido SM, Bhanap P, et al. Commensal-derived tryptophan metabolites fortify the skin barrier: insights from a 50-species gnotobiotic model of human skin microbiome. Cell Chem Biol. 2025;32(1):P111-P125.E6. doi:10.1016/j.chembiol.2024.12.007
13. Natarelli N, Gahoonia N, Sivamani RK. Bacteriophages and the microbiome in dermatology: the role of the phageome and a potential therapeutic strategy. Int J Mol Sci. 2023;24(3):2695. doi:10.3390/ijms24032695
14. Nakatsuji T, Chiang H, Jiang SB, Nagarajan H, Zengler K, Gallo RL. The microbiome extends to subepidermal compartments of normal skin. Nat Commun. 2013;4:1431. doi:10.1038/ncomms2441
15. Nakatsuji T, Cheng JY, Gallo RL. Mechanisms for control of skin immune function by the microbiome. Curr Opin Immunol. 2021;72:324-330. doi:10.1016/j.coi.2021.09.001
16. Dokoshi T, Chen Y, Cavagnero KJ, et al. Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice. Nat Commun. 2024;15:3009. doi:10.1038/s41467-024-47072-3
17. Kline SN, Feller LE, Saito Y, et al. Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march. Cell Reports. 2025;44(8):116054. doi:10.1016/j.celrep.2025.116054
18. Wang G, Sweren E, Liu H, et al. Bacteria induce skin regeneration via IL-1β signaling. Cell Host Microbe. 2021;29(5):777-791.e6. doi:10.1016/j.chom.2021.03.003
19. Durack J, Piceno Y, Vuong H, et al. Yanomami skin microbiome complexity challenges prevailing concepts of healthy skin. Nat Comm. 2025;16:5542. doi:10.1038/s41467-025-60131-7
20. Roslund MI, Puhakka R, Grönroos M, et al. Biodiversity intervention enhances immune regulation and health-associated commensal microbiota among daycare children. Sci Adv. 2020;6(42):eaba2578. doi:10.1126/sciadv.aba2578.
21. Metwaly A, Kriaa A, Hassani Z, et al. A consensus statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research. Nat Rev Gastroenterol Hepatol. 2025;22:343-356. doi:10.1038/s41575-025-01041-3
22. Shahid U. Microbiome-guided precision medicine: mechanistic insights, multi-omics integration, and translational horizons. J Precis Med: Health Dis. 2025;3:100018. doi:10.1016/j.premed.2025.100018

Sent from my iPhone

Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

Please excuse the shortness of this message, as it has been sent from
a mobile device.